Atherosclerosis and ischemic heart disease

Question 1

What arteries are most commonly affected by atherosclerosis?

Answer 1

elastic arteries - aorta, carotid and iliac arteries
can also occur in large/medium muscular arteries (coronary arteries)
commonest site= aorta and coronary vessels

Question 2

What is the atheromatous plaque initially formed of and where do they initially start?

Answer 2

lipid matrix within the intima

Question 3

Why are atheromatous plaques thought to form?

Answer 3

due to a chronic inflammatory response to chronic endothelial injury - lipid will cause inflammation and extracellular matrix formation - narrows the vessel lumen and can progress to affect the media

Question 4

What are plaques formed of?

Answer 4

composed of smooth muscle and inflammatory cells, lipids, connective tissue, extracellular matrix and a fibrous cap

Question 5

What do stable and unstable plaques have?

Answer 5

thick fibrous cap for stable plaques

unstable plaques lack a thick cap and therefore are much more likely to rupture

Question 6

When does the formation of atherosclerosis begin?

Answer 6

in childhood with the appearance of fatty streaks within vessels
- plaques then develop throughout life typically becoming symptomatic in middle age or later

Question 7

What are the complications of atherosclerotic plaques?

Answer 7

MI
Chronic ischemic heart disease 
Stroke
Aneurysm 
Gangrene of extremities 
Gut ischaemia

Question 8

Why do the complications of atherosclerotic plaques occur?

Answer 8

vessel narrowing as plaque size increases, there is hemorrhage into the plaque or thrombi form on its surface

Question 9

What are non-modifiable risk factors for atherosclerosis?

Answer 9

age
males
family hx
genetic abnormalities

Question 10

What are modifiable risk factors for atherosclerosis?

Answer 10

hyperlipidemia
hypertension
smoking
diabetes

Question 11

When does ischemic heart disease occur?

Answer 11

imbalance between supply and demand of the heart for oxygenated blood

Question 12

What is the vast majority of cases of IHD due to and what are some other causes?

Answer 12

atherosclerosis of coronary arteries but can also be due to congenital heart disease, anaemia and lung disease

Question 13

What makes IHD worse?

Answer 13

hypertrophy, hypertension, hypoxemia and increased heart rate

Question 14

What factors need to be taken into account in terms of determining risk of developing IHD?

Answer 14

1) Number of vessels involved
2) distribution and degree of narrowing of those vessels
it is increased when atheroma are unstable

Question 15

What are the main ways of preventing the development of IHD?

Answer 15

1) Prevention and lifestyle modification

2) therapeutic interventions = CCU, angioplasty, stents, CABGs and improved arrhythmia control

Question 16

What four syndromes can be caused by IHD?

Answer 16

MI
angina
chronic ischemic heart disease (leads to HF and fibrosis)
sudden cardiac death

Question 17

What is the difference between MI and angina?

Answer 17

necrosis
- MI there will be myocyte necrosis leading to elevated creatinine kinase and troponin
remain high long after the cardiac event itself

Question 18

What is the definition of critical stenosis in IHD and what does it mean?

Answer 18

• occurs when there is at least a 75% reduction in the cross sectional area of the vessel
• compensatory vasodilation will no longer be sufficient to meet cardiac demands and angina occurs

Question 19

What vessels tend to be involved in critical stenosis in IHD?

Answer 19

Normally more than one vessel
- typically proximal left anterior descending, proximal left circumflex and /or entire length of the right coronary artery

Question 20

What are the most dangerous lesions in IHD?

Answer 20

Those in which there is 50-75% stenosis with a lipid rich core and minimal fibrous cap = lesion is unstable but below critical stenosis
so pt will have had no angina and therefore no collateral angiogenesis will have taken place
- sudden rupture of the plaque can be the first ischemia heart faces and this will be very damaging

Question 21

What are the 2 main forms of MI as a complication of IHD?

Answer 21

1) Transmural MI = infarction of the full thickness of the heart wall - usually associated with acute thrombosis or vessel occlusion and sometimes vasospasm or emboli (territory supplied by a single vessel becomes infarcted)
2) subendocardial MI - affects the inner third to half of the myocardium

Question 22

What are the 3 main coronary arteries affects in MIs?

Answer 22

1) left anterior descending = supplies apex, anterior left ventricle, and anterior inter ventricular septum
2) left circumflex = supplies lateral left ventricle
3) right coronary artery = supple the posterior left ventricle, posterior inter ventricular septum and right ventricle

Question 23

When does histological evidence of an MI become apparent?

Answer 23

after around 4 hours and this can be seen macroscopically from around 12 hours

Question 24

What is necessary to preserve heart following MI?

Answer 24

Preserve as much heart function as possible reperfusion (thrombolysis) is essential

• salvage sub-lethally injured myocytes and minimize infarct size
• but vessel damage means there will be hemorrhage and there may be some reperfusion injury due to free radical formation

Question 25

What is meant by stunned myocardium?

Answer 25

despite thrombolysis some myocytes may not function for several days

Question 26

What are the complications of MI?

Answer 26

- contractile dysfunction = HF and cardiogenic shock - arrhythmia - rupture of myocardium into pericardium across inter ventricular septum causing L-R shunts and rupture of papillary muscles = mitral regurgitation - pericarditis - mural thrombosis - ventricular aneurysm - papillary muscle dysfunction leading to mitral regurgitation - progressive HF

Question 27

When and why does pericarditis occur following MI?

Answer 27

Often occurs early following MI due to autoimmune dresseler syndrome

Question 28

When does congestive cardiac failure occur?

Answer 28

when there is a failure of the heart's pump mechanism - adaptive mechanisms to prevent or postpone total heart failure relate to starling's law - there is action to increase preload as well as contractile force

Question 29

What is hypertrophy/cardiomegaly?

Answer 29

increase in the weight and wall thickness of the heart due to an increase in myocyte size - increase in chamber size, dilation, increases preload

Question 30

What neurohormonal mechanisms occur in hypertrophy?

Answer 30

activation so NA is released to increase HR and activation of RAAS system and ANP release to increase blood pressure though fluid retention - attempt to increase oxygenated blood output

Question 31

What is the difference between systolic and diastolic failure in HF and which is more common?

Answer 31

Systolic function failure = heart cannot contract enough - more common Diastolic function failure = chamber walls are too still and unable to stretch and fill with blood

Question 32

What happens in left sided HF?

Answer 32

Congestion of blood in the pulmonary circulation = pulmonary edema and organ ischemia

Question 33

What happens in right sided HF?

Answer 33

Congestion of blood in the systemic circulation = peripheral edema, congestion of organs, ascites and pleural effusion

Question 34

Which is more common left or right sided HF?

Answer 34

Left sided is more common but it can lead to right sided due to increased heart after load Pure right heart failure = cor pulmonale = rare

Question 35

What are the characteristics of hypertensive heart disease?

Answer 35

diagnosed through evidence of concentric left ventricular hypertrophy (in response to pressure overload) and pathological evidence of hypertension

Question 36

How can hypertensive heart disease present?

Answer 36

present with AF due to left atrial enlargement, congestive cardiac failure or asymptomatic ECG screening

Question 37

What is different in terms of the chambers in hypertensive heart disease compared to congestive heart failure?

Answer 37

no dilation of chambers in hypertensive heart disease increase in wall thickness and heart weight - thickened wall impairs diastolic function, leading to left atrial enlargement

Question 38

Histologically what does hypertensive heart disease look like?

Answer 38

increased myocyte size and nuclear size as well as interstitial fibrosis

Question 39

What is cor pulmonale?

Answer 39

pulmonary hypertensive heart disease therefore affecting right side of the heart Secondary to pulmonary hypertension- this can be an abnormality of the lungs of pulmonary vasculature

Question 40

What does cor pulmonale not include?

Answer 40

doesn't include pulmonary hypertension due to congenital heart disease of left heart diseases

Question 41

What happens when there is an acute increase in pulmonary blood pressure ? e.g. pulmonary embolus

Answer 41

leads to marked dilation of right ventricle with no hypertrophy

Question 42

What happens when there is a chronic increase in pulmonary pressure?

Answer 42

prolonged pressure overload causes right ventricular hypertrophy