Atherosclerosis and ischaemic heart dieases Flashcards
What is atherosclerosis?
Which arteries does it tend to affect?
- Contributes more mortality than any other disease in Western World
- more than 1/2 of all deaths
- Serious morbitity as well
- Effects
- elastic arteries – Aorta, Carotid and Iliac arteries
- Large and medium muscular arteries – coronary and popliteal arteries.
- Intimal lesion – atheromatous plaques
What is the distribution of atherosclerotic plaques?
- Abdominal aorta (more prominent around ostia) (most frequent)
- Coronary arteries
- Popliteal arteries
- Descending thoracic aorta
- Internal carotid arteries
- Circle of Willis (least frequent)
ATHEROSCLEROSIS
When does it start?
What complications can it cause?
Fatty streak in children
Atheromatous plaques develop throughout life
Symptomatic middle age or later
CONSEQUENCES MI / chronic IHD / sudden death Stroke / CVA AAA Gangrene of legs Gut ischaemia
Narrowing – plaque size, overlying thrombus, haemorrhage into
Dilation (aneurysm) – rupture, mural thrombi
What is contained in an ATHEROMATOUS PLAQUE
- fibrous cap
- cells (smooth muscle and inflammatory)
- lipid
- connective tissue and extracellular matrix
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STABLE VS UNSTABLE PLAQUE
What is the difference between them?
Stable plaque – thick fibrous cap (more stable)
Unstable plaque – no thick cap at risk of rupture / fissure emboli +/- thrombosis
RISK FACTORS FOR ATHEROSCLEROSIS
What are the modifiable and non modifiable risk factors?
NON MODIFIABLE Increasing age Male gender Family history Genetic abnormalities
MODIFIABLE Hyperlipidaemia Hypertension Smoking Diabetes
PATHOGENESIS OF ATHEROSCLEROSIS
“RESPONSE TO INJURY” HYPOTHESIS
CHRONIC INFLAMMATORY RESPONSE OF ARTERIAL WALL INITIATED BY CHRONIC ENDOTHELIAL INJURY
Ischaemic heart disease
Define myocardial ischaemia.
90% it is due to?
Rest are due to?
What 4 things aggrivate IHD?
What affect the risk of developing ischaemic heart disease?
How can it be decreased?
MYOCARDIAL ISCHAEMIA = imbalance between supply and demand of the heart for oxygenated blood
90% due to ATHEROSCLEROSIS of coronary arteries (coronary artery disease) Rest – congenital heart disease, anaemia, lung disease
Aggravated by: hypertrophy, hypotension, hypoxaemia, increased heart rate
Risk of developing IHD depend on: number of vessels involved, distribution, degree of narrowing, stable or unstable plaques
Leading cause of death in industrialised nation
Decrease by 1. prevention (modification of risk factors) smoking, hypercholesterolaemia, sedentary life style
- Therapeutic advances new medications, CCU(coranary care unit), angioplasty, stents, CABGs, improved control of arrhythmias
What are 4 syndrome of Ischaemic heart disease?
What is the difference between angina and MI?
In MI how long does it take for troponins and CK to rise?
Myocardial infarction (MI)
Angina Pectoris
Chronic IHD
Sudden cardiac death
Angina Ischaemic episode short enough no necrosis
MI - Myocyte necrosis, Elevated enzymes – creatinine kinase, Elevated cardiac specific proteins – troponins Both rise 4-8 hrs. CK 3 days. Troponins 7-10 days
Define critical stenosis?
Critical stenosis = at least 75% reduction of cross-sectional area
compensatory vasodilation not enough to meet increased demands
1, 2, 3 or more vessels involved. Usually >1
Prox LAD, Prox LCX, entire length RCA
Most dangerous lesions 50-75% stenosis with lipid rich core and minimal fibrous cap. Alone do not produce angina – but risk of acute plaque change.
Not developed collaterals ? Lack of preconditioning (small ischaemia to heart can protect myocardium)
What is the difference between transmural and subendocardial MI
TRANSMURAL = full thickness of the wall
Usually associated with acute thrombosis / occlusion of vessel. Occasionally related to vasospasm or emboli, distribution of a single artery
SUBENDOCARDIAL – inner 1/3 – 1/2 myocardium may extend beyond the perfusion territory of a single artery subendocardial zone = least well perfused so most at risk of reduced corionary flow Usually critical stenosis but no acute plaque change
What does the following coronary arteries supply?
Left anterior descending
Left circumflex
Right Coronary artery
LAD apex, ant wall LV, ant IVS
- LCX lat LV not apex
- RCA inf-post wall LV, post IVS, RV
When would hisological changes be seen and when will macropscopic changes be seen in MI?
Why is thrombolysis done?
What can happen if thrombolysis is done which could cause a new injury?
What is a stunned myocardium?
What is preconditioning?
Histologically – see from
4 hrs
Macroscopically – see from 12 hrs some dyes allow to see earlier
Early reperfusion (thrombolysis) – salvage sublethally injured myocytes and minimise infarct size. Haemorrhage into area.
Reperfusion induces an element of “new” injury – REPERFUSION INJURY. Free radicals.
Despite salvage from death – myocytes may not function for several days = “STUNNED MYOCARDIUM”
Repetitive short lived ischaemia may be protective “PRECONDITIONING” ?mechanisms
What ar ethe complications of MI?
Contractile dysfunction = heart failure = cardiogenic shock
Arrhythmias
Myocardial rupture Free wall – tamponade IVS – left to right shunt papillary muscle – acute severe mitral regurgitation
Pericarditis early or several weeks (Dressler syndrome = autoimmune)
Mural thrombus = at risk of embolising
Ventricular aneurysm
Papillary muscle dysfunction – MR
Progressive late heart failure (
What is the normal size of a normal heart in a female and a male?
what happens in increased size?
What is it called if the chamber size increases?
What are the cardiac myocyte responsible for?
What cells are important for conduction in the heart?
- Pump
- 250-300g females, 300-350g males
- Increased size (weight / wall thickness) = hypertrophy / cardiomegaly
- Increased chamber size = dilation •Cardiac myocyte = cell of contraction
- Specialised myocytes for conduction – Sinoatrial node, atrioventricular node and bundle of His
what happens in left heart failure? what is affected?
LEFT – usual form, occurs in most forms of heart disease
PULMONARY OEDEMA
ORGAN ISCHAEMIA – impaired renal function
what happens in right heart failure?
RIGHT usually occurs secondary to left heart failure Pure right heart failure uncommon – cor pulmonale
Peripheral oedema
Congestion of organs
Ascites / pleural effusion
SYSTEMIC HYPERTENSIVE HEART DISEASE
diagnostic criteria
What is the gross morphology
What is seen in histology?
DIAGNOSTIC CRITERIA
- Left ventricular hypertrophy (concentric) +
- History / pathological evidence of hypertension
Even prolonged mild hypertension hypertrophy
PRESENTATION Asymptotic, ECG / echocardiograph, Atrial fibrillation (left atrial enlargement), CCF
GROSS MORPHOLOGY Circumferential LV hypertrophy, No dilation of LV, increase heart weight, Thick wall
Thick wall = stiff -> impaired diastolic filling -> left atrial enlargement
HISTOLOGY: increased size of myocyte, Increased nuclear size, interstitial fibrosis
What is cor pulmonale?
What is th difference between acute and chronic cases?
Pulmonary hypertensive heart disease (RIGHT SIDED)
Secondary to pulmonary hypertension - abnormality of lungs / pulmonary vasculature.
EXCLUDE pulmonary hypertension 2o to congenital heart disease, diseases of the left side of the heart
ACUTE - sudden increase in pulmonary blood pressure eg massive pulmonary embolus marked dilation of the right ventricle no hypertrophy CHRONIC - prolonged pressure overload right ventricular hypertrophy
