Atherosclerosis and ischemic heart disease Flashcards
What arteries are most commonly affected by atherosclerosis?
elastic arteries - aorta, carotid and iliac arteries
can also occur in large/medium muscular arteries (coronary arteries)
commonest site= aorta and coronary vessels
What is the atheromatous plaque initially formed of and where do they initially start?
lipid matrix within the intima
Why are atheromatous plaques thought to form?
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
What are plaques formed of?
composed of smooth muscle and inflammatory cells, lipids, connective tissue, extracellular matrix and a fibrous cap
What do stable and unstable plaques have?
thick fibrous cap for stable plaques
unstable plaques lack a thick cap and therefore are much more likely to rupture
When does the formation of atherosclerosis begin?
in childhood with the appearance of fatty streaks within vessels
- plaques then develop throughout life typically becoming symptomatic in middle age or later
What are the complications of atherosclerotic plaques?
MI Chronic ischemic heart disease Stroke Aneurysm Gangrene of extremities Gut ischaemia
Why do the complications of atherosclerotic plaques occur?
vessel narrowing as plaque size increases, there is hemorrhage into the plaque or thrombi form on its surface
What are non-modifiable risk factors for atherosclerosis?
age
males
family hx
genetic abnormalities
What are modifiable risk factors for atherosclerosis?
hyperlipidemia
hypertension
smoking
diabetes
When does ischemic heart disease occur?
imbalance between supply and demand of the heart for oxygenated blood
What is the vast majority of cases of IHD due to and what are some other causes?
atherosclerosis of coronary arteries but can also be due to congenital heart disease, anaemia and lung disease
What makes IHD worse?
hypertrophy, hypertension, hypoxemia and increased heart rate
What factors need to be taken into account in terms of determining risk of developing IHD?
1) Number of vessels involved
2) distribution and degree of narrowing of those vessels
it is increased when atheroma are unstable
What are the main ways of preventing the development of IHD?
1) Prevention and lifestyle modification
2) therapeutic interventions = CCU, angioplasty, stents, CABGs and improved arrhythmia control
What four syndromes can be caused by IHD?
MI
angina
chronic ischemic heart disease (leads to HF and fibrosis)
sudden cardiac death
What is the difference between MI and angina?
necrosis
- MI there will be myocyte necrosis leading to elevated creatinine kinase and troponin
remain high long after the cardiac event itself
What is the definition of critical stenosis in IHD and what does it mean?
- 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
What vessels tend to be involved in critical stenosis in IHD?
Normally more than one vessel
- typically proximal left anterior descending, proximal left circumflex and /or entire length of the right coronary artery
What are the most dangerous lesions in IHD?
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
What are the 2 main forms of MI as a complication of IHD?
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
What are the 3 main coronary arteries affects in MIs?
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
When does histological evidence of an MI become apparent?
after around 4 hours and this can be seen macroscopically from around 12 hours
What is necessary to preserve heart following MI?
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
What is meant by stunned myocardium?
despite thrombolysis some myocytes may not function for several days
What are the complications of MI?
- 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
When and why does pericarditis occur following MI?
Often occurs early following MI due to autoimmune dresseler syndrome
When does congestive cardiac failure occur?
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
What is hypertrophy/cardiomegaly?
increase in the weight and wall thickness of the heart due to an increase in myocyte size
- increase in chamber size, dilation, increases preload
What neurohormonal mechanisms occur in hypertrophy?
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
What is the difference between systolic and diastolic failure in HF and which is more common?
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
What happens in left sided HF?
Congestion of blood in the pulmonary circulation = pulmonary edema and organ ischemia
What happens in right sided HF?
Congestion of blood in the systemic circulation = peripheral edema, congestion of organs, ascites and pleural effusion
Which is more common left or right sided HF?
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
What are the characteristics of hypertensive heart disease?
diagnosed through evidence of concentric left ventricular hypertrophy (in response to pressure overload) and pathological evidence of hypertension
How can hypertensive heart disease present?
present with AF due to left atrial enlargement, congestive cardiac failure or asymptomatic ECG screening
What is different in terms of the chambers in hypertensive heart disease compared to congestive heart failure?
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
Histologically what does hypertensive heart disease look like?
increased myocyte size and nuclear size as well as interstitial fibrosis
What is cor pulmonale?
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
What does cor pulmonale not include?
doesn’t include pulmonary hypertension due to congenital heart disease of left heart diseases
What happens when there is an acute increase in pulmonary blood pressure ? e.g. pulmonary embolus
leads to marked dilation of right ventricle with no hypertrophy
What happens when there is a chronic increase in pulmonary pressure?
prolonged pressure overload causes right ventricular hypertrophy
