CAD Flashcards
NSTEMI
non- ST segment elevation myocardial infarction
some flow restriction - atheroma is there
present with angina
mortality
1 in 5 men and 1 in 7 women will die of CAD
myocardial ischaemia
occurs when there is an imbalance between the demand of the myocardium for oxygen and nutrients and what is being given to it
cardiogenic shock can also lead to MI
inadequate perfusion due to cardiac dysfunction
how may coronary blood flow to the myocardium be reduced due to obstruction?
atheroma thrombosis spasm embolus coronary ostial stenosis coronary arteritis
reduced coronary blood flow to myocardium - other
anaemia
carboxyhaemoglobulinaemia
hypotension
** there may also be a higher demand for oxygen and nutrients due to an increase in CO - eg thyrotoxicosis or myocardial hypertrophy
common symptoms
> angina is a clinical diagnosis of CAD
chest pain is taken very seriously
need to be tested for coronary obstructive lesions
what can cause injury to the initial intimal endothelial injury ? thus triggering atherogenesis
mechanical shear stress (ie from hypertension)
biochemical abnormalities (ie elevated LDL levels, diabetes)
immunological factors (ie free radicals from smoking)
inflammation
genetic alteration
risk factors (three parts)
age - increased incidence in both genders with increased age
gender - men more likely
race
Fx
>modifiable major risk factors = serum cholesterol smoking diabetes hypertension lack of exercise coag. factors obesity gout soft water heavy alcohol consumption
> patients with peripheral vascular disease have x2-x4 increased risk of CAD, stroke or heart failure
after an initial MI there is increased risk of heart failure and stroke x3 - x6
after stroke MI and heart failure is increased x2
tests !
exercise ECG ! less clear interpretation with women
perfusion scanning ! bad bc. radiation dose but good bc. non-invasive
CTCA ! good bc. non-invasive but some radiation and less precise than invasive CA
angiography !
CT scan !
pathophysiology of coronary atherosclerosis
its a complex inflammatory process !!
injury to the endothelial wall means that lipids - cholesterol is more likely to stick to the tear in the wall they then oxidise which is bad
so white cells/macrophages come along and phagocytose the cholesterol and become a foam cell
these then disintegrate essentially and this forms the basis of the atheroma - they look like fatty streaks
at this stage it would be a transitional plaque !
release of cytokines by monocytes, macrophages or the damaged endothelium promotes further accumulation of macrophages as well as smooth muscle cell migration and proliferation
this proliferation causes further thickening
collagen is produced by the smooth muscle cells at this point it would be the advanced or raised fibrolipid plaque
this may grow and encroach on the lumen or become unstable and undergo thrombosis and produce and obstruction becoming a complicated plaque !
»thrombosis on the plaque … see superficial endothelial injury and deep endothelial fissuring
primary vs secondary prevention of CAD
primary - this would be how to prevent atherosclerosis in coronary arteries
secondary - treating a current atheroma in the artery
»the objective of both is to prevent/reduce the incidence of first or recurrent clinical events die to CAD ischaemic stroke
familial hypercholesterolaemia
patients who have a total cholesterol concentration of more than 7.5mmol/L and a family history of premature CAD
lifestyle modifications
reduced fat intake diet
dietary cholesterol intake of less than 300mg a day
saturated fats should be replaced with mono/poly unsaturated fats
reduce sugar / refined sugar intake
aim to eat five portions of fruit and vegetables a day
exercise ! 150min of moderate exercise or 75min of vigorous
no more than 14 units a week
