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September lectures yr 3 (2018) > Atherosclerosis and ischemic heart disease > Flashcards

Atherosclerosis and ischemic heart disease Flashcards

1
Q

What arteries are most commonly affected by atherosclerosis?

A

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

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2
Q

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

A

lipid matrix within the intima

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3
Q

Why are atheromatous plaques thought to form?

A

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

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4
Q

What are plaques formed of?

A

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

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5
Q

What do stable and unstable plaques have?

A

thick fibrous cap for stable plaques

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

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6
Q

When does the formation of atherosclerosis begin?

A

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

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7
Q

What are the complications of atherosclerotic plaques?

A 
MI
Chronic ischemic heart disease 
Stroke
Aneurysm 
Gangrene of extremities 
Gut ischaemia
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8
Q

Why do the complications of atherosclerotic plaques occur?

A

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

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9
Q

What are non-modifiable risk factors for atherosclerosis?

A

age
males
family hx
genetic abnormalities

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10
Q

What are modifiable risk factors for atherosclerosis?

A

hyperlipidemia
hypertension
smoking
diabetes

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11
Q

When does ischemic heart disease occur?

A

imbalance between supply and demand of the heart for oxygenated blood

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12
Q

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

A

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

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13
Q

What makes IHD worse?

A

hypertrophy, hypertension, hypoxemia and increased heart rate

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14
Q

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

A

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

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15
Q

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

A

1) Prevention and lifestyle modification

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

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16
Q

What four syndromes can be caused by IHD?

A

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

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17
Q

What is the difference between MI and angina?

A

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

18
Q

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

A
  • 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
19
Q

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

A

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

20
Q

What are the most dangerous lesions in IHD?

A

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

21
Q

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

A

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

22
Q

What are the 3 main coronary arteries affects in MIs?

A

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

23
Q

When does histological evidence of an MI become apparent?

A

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

24
Q

What is necessary to preserve heart following MI?

A

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
25
Q

What is meant by stunned myocardium?

A

despite thrombolysis some myocytes may not function for several days

26
Q

What are the complications of MI?

A
  • 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
27
Q

When and why does pericarditis occur following MI?

A

Often occurs early following MI due to autoimmune dresseler syndrome

28
Q

When does congestive cardiac failure occur?

A

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

29
Q

What is hypertrophy/cardiomegaly?

A

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

30
Q

What neurohormonal mechanisms occur in hypertrophy?

A

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

31
Q

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

A

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

32
Q

What happens in left sided HF?

A

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

33
Q

What happens in right sided HF?

A

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

34
Q

Which is more common left or right sided HF?

A

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

35
Q

What are the characteristics of hypertensive heart disease?

A

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

36
Q

How can hypertensive heart disease present?

A

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

37
Q

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

A

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

38
Q

Histologically what does hypertensive heart disease look like?

A

increased myocyte size and nuclear size as well as interstitial fibrosis

39
Q

What is cor pulmonale?

A

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

40
Q

What does cor pulmonale not include?

A

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

41
Q

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

A

leads to marked dilation of right ventricle with no hypertrophy

42
Q

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

A

prolonged pressure overload causes right ventricular hypertrophy

September lectures yr 3 (2018) (56 decks)

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