ischemic heart disease Flashcards
ischameic heart disease is a Huge problem , most common serious life-threatening disease Western World
1- Review — of
– Atherosclerosis
– Diabetes
– Hypertension
– Obesity
– Cigarette smoking
– Thrombosis
* Review — of
– Heart and Circulation
– Haemostasis &
Coagulation cascade
pathology
physiology
myocardial oxygen demand and supply:
* Demand
– —
– —
– —
* Supply
– —
– —
( so basically high demand , low supply + chrck photos )
rate
contractility
tension
oxygenated blood
coronary artery flow
coronary artries - epicardial:
* Left coronary artery-
1.5cms → — & (L) — .
* LAD supplies the — , — — of — & — wall of —
* Right coronary artery
classically the — wall
“ —” in ECG.
* right coronary artery usually
supplies the — of the—
interventricilar LAD and L circumflex
apex
anterior 2/3 of septum
anterior wall of LV
posterior
inferior
posterior of septum
Ischaemic heart disease [IHD]
Myocardial Oxygen — not matched by —
Clinical syndromes which reflecting varying pathologies
* —
– Stable
– Unstable
* —-
* — ischaemic heart disease
demand
supply
Angina pectoris
myocardial infraction
chronic
1- IHD - stable angina:
* Usually, — caused by — and relieved by — and
– often not— .
* Reflects “Significant” vessel — → —
* One vessel > 75% — or 2 > 50% …usually
* Assessment via — . Often if autopsy done →microscopic myocardial fibrosis. Why?
* Angina may be worsened by — or increased— i.e. —
* may reflect important — disease
2- IHD - unstable angina :
* Stable angina with recent progressively increasing —
* Precipitated with progressively – effort
– Often occurs at – & tends to be of more — duration.
* Induced by disruption of an — (plaque— ) & — .
* Increased risk of subsequent —
chest pain
excerise
rest
clear cut
narrowing
atheroma
stenosis
angiography
anemia
cardiac mass
hypertrophy
non cardiac
frequency
less effort
rest
prolonged
athersolotic plaque
rapture
secondary thrombus
acute Mi
- IHD - sudden cardiac death:
- Defined as death within — onset of symptoms though often virtually — .
– Can arise as a result of : - Sudden large — on a ruptured
atheromatous plaque - Secondary to an – in chronic ischaemic heart disease
as defined above. - 50% – before arrival in hospital
– Mechanism – —
– Coronary — e.g. cocaine use - rare
2- IHD - myocardial infraction: - Myocardial — due to — blood supply
- Usually reflects — coronary artery — evolving to tissue death
– — process and can be reduced by coronary – following “—-” - Certain plaques more likely to thrombose – — rich with — cap → —
- —- stabilises plaques
60 min
instantaneous.
coronary thrombosis
arrthymua
dead
ventricular fibrillation
arterial spasm
necrosis
reduced
unrelieved
occlusion
dynamic
repercussion
stenting
lipid
fibrous
cracks
statins
- ischemic heart disease IHD - myocardial infraction clinical presentation:
- Crushing — chest pain, — by rest; accompanied by weakness, sweating, nausea & vomiting
– Radiates commonly to – shoulder and — - May be described as —
- Can be painless [silent] – old / diabetes
- Pain may be atypical e.g. abdominal - teeth - shoulder etc.
- May be “silent” present as heart failure (esp in elderly)
arrhythmia – confusion – weakness. - Need a – index of suspicion
- pathology :
- Coronary atheroma –> plaque – and subsequent — initiates – – possibly reversible for —
- Necrosis of myocardium begins – after — & progresses from — through – thickness of the myocardium to —
zone. (—-)
– Why is it subendocardial? - Most untreated episodes of ischaemia cause — > —-
- NB Subendocardial (AKA Non ST-elevation MI–NSTEMI) infarction more likely
in incomplete artery occlusion or may develop in prolonged shock.
central
unrelieved
left shoulder and jaw
indigestion
high
repture
thrombosis
ichemia
6-12 hours
30 min
occlusion
subendocardial myocardium
full thickness
pericardial
transmural infracts
trasmural infraction
pathogensis of coronary artery occlusion:
* Plaque – / –
* Exposure of – , smooth muscle —
* – generation and fibrin platelet —
* Thrombus in the atheromatous plaque with repair
-Plaque rupture with secondary thrombosis may give rise to — or —
- myocardial infraction diagnosis:
* Clinical
* – (— ):
– quick, easy and gives information about site and vessel
involved as well as information about arrhythmias.
* Lab Evaluation :
– — and — used most commonly.
– Also, MB fraction of —
rapture / fissure
lipid
foam cells
thrombin
aggregates
myocardial failure or fatal arrhythmia
ECG ( EKG)
Troponin-I (TNI) & Troponin-T
creatine kinase ( enzyme )
1- troponin advantages:
(1) — specific.
(2) — elevation x — days.
* Enzyme levels give some idea of — of infarct:
– Extent depends on — of vessel obstruction
– Significance of –
– — of myocardial hypertrophy
– Presence of – coronary circulation.
2- cardiac tropinins :
* – proteins of — in – muscle – engage with —
-Certain subtypes of troponin (I and T) are indicators of — to the
myocardium and can be measured in the blood by — techniques
motor
persistent
7-14 days
extent
location
vessel
degree
collateral
regulatory
actin filmanrtd
cardiac
calcium
damage
immunoassay
troponin levels - not specific:
Other conditions associated with raised troponins (any cause of — )
* Cardiac surgery
* Cardiac contusion
* Myocarditis
* Cardiomyopathy & HOCM
* Chemotherapy
* Renal disease
* Poly – dermato-myositis
- Troponins are a marker of all heart muscle cell –
myocardial necrosis
necrosis
myocardial infraction microscopic and gross pathology:
Up to — no microscopic change in myocardium
But patient may Be Dead – problem for pathologist & cause of Death !!
* Day 1: Myocardium
Coagulation — with— and wavy fibres. — vessels – — .
Macroscopically - — Firm
* Day 2 – 7:
Beside necrotic area –— – neutrophils and oedema. If marked
can get fever and raised — (bad prognosis).
Macroscopically – Soft – — tissue.
* Day 7 – 14:
Ongoing — process with — of dead tissue and — tissue at edges.
Macroscopic – depressed area with — edges.
* Week 2-8:
Evolving — and decreasing — .
Macroscopic– – tissue
* Week 8:
— fibrosis
Macroscopic depressed — myocardium and –
10 hours
necrosis
hypereosinophilia
dead
haemorrhage
dark red
inflammation
WCC
soft yellowish - tan tissue
repair
resorption
granulation
depressed w red edges
firbosis
vascularity
grey white
dense
thinned
scar
( check slide 24-30 )
healing myocardium post MI summary:
Macroscopy
* 0-12 hrs. None
* 12-24 hrs. Pallor
* 1-3 d –
* 4-7d —
* 7-14d —
* >2 weeks — scar
Microscopy
* Nil
* Coagulative necrosis /
contraction bands
* Above + neutrophils
* Above + macrophages
* Above + granulation tissue
* Fibrosis (Scar)
- most important point:
* Cause of MI is almost always — due to – caused by — of an
atheromatous plaque leading to partial or complete occlusion of the artery
* Evaluation of the heart at autopsy includes
– Assessment of
* —
* –
hyperaemic
pale yellow
red purple
grey white
coronary artery occlusion
thrombosis
rupture
coronary artries and myocardium
rare causes of contrary occlusion:
* Vasculitis
* Thrombus due to –
* – eg Cocaine or other drugs
* – – coronary dissection
* Almost never —
- what other conditions of the heart can lead to MI:
* Massive — as more muscle mass to be oxygenated
* – [severe]
- summary of MI complications:
* Sudden death
– What causes this?
* Arrhythmias Within 48 hours usually (posterior MI usually)
* Left ventricular failure & pulmonary oedema
* Cardiogenic shock
* Ventricular rupture & haemopericardium (After 4 days)
* Chordae tendineae - papillary muscle rupture (rare)
* Left ventricle Aneurysm formation and +/- emboli
* Pericarditis (acute or chronic) & Dressler’s syndrome
hypercoagulabity
Vasospasm
trauma
emboli
hypertrophy and anemia
- sudden deaths in MI most frequent causes:
- –
– — - Especially — - — MI (on ECG)
- Cardiac — & Haemopericardium —> Cardiac —
- muscle rupture post MI:
- If through — (usually
after 4 days)- haemopericardium - If — ventricular septal defect
- —– acute
valve dysfunction intractable heart failure.
-Why? Valve won’t close
properly
arrhythmias
ventricular fibirllation
posterior - inferior MI
rapture
tamponade
free wall
septum
papillary muscles
why does MI cause LVF:
Myocardial cell death cause — which leads to — failure (LVF)
* Signs of LVF:
– Mild:
* sinus – but — BP and – tissue perfusion
– Moderate:
* — with clinical/radiological evidence of pulmonary
oedema.
– Severe:
* Cardiogenic shock, hypotension, poor tissue perfusion and
markedly decreased ejection fraction on ECHO
pump failure
left ventricular failure
tachycardia
normal
good
dyspnea
- pulmonary oedema:
- Pulmonary oedema is – (transudate) in the – spaces
- Due to – or — failure which causes pulmonary — hypertension
- Increased — pressure in pulmonary capillaries
- Pulmonary oedema (fluid in alveolar spaces)
- Dyspnoea
- Spectrum from mild left ventricular failure to intractable hypotension known as — very poor outlook
- Pump problems are particularly associated with — MI
- Conduction difficulties with — MI.
- Combination of both suggests very extensive myocardial injury with ominous prognosis
fluid
alveolar
left artel or left ventricular
venous
hydrostatic
cardiogenic shock
anterior
posterior
muscle replacement and weakig post MI:
* — / — :
– — increasing risk of chronic
heart failure, arrhythmias and
mural thrombosis.
– — in aneurysm sac → systemic
emboli.
* Dressler’s syndrome ( — )
fibrosis/ scarring
ventricular aneurysm
mural thrombosis
pericarditis
1- chronic ishcemic heart disease:
* Clinical
– Angina & Progressive Heart
Failure [see HF lecture]
* Pathology
– usually big heart, with combination of hypertrophy, dilatation, narrowed
coronary arteries and myocardial
fibrosis.
* Summary
– crucial topic – primary prevention
vital.
– e.g. non invasive coronary imaging
– statin treatment, angioplasty and
improvements in heart failure
management.
– Perhaps heart transplant in the
future
- Acute coronary syndrom ACS:
Vulnerable Lipid Laden Plaques:
disruption or erosion of — –> platelt — and — generation –> insuffienct — blood supply —> ACS which can be STEMI or NSTEMI
fibrous cap
aggregation + thrombin
collateral
1- STEMI:
Cardiac Emergency - Rush to Catheter Laboratory
Lost time means loss of – / – function
- pathophysiology : occlusive thrombus
- presnetation: elevated enzyme
- goal: reperfusiin
* May be no — circulation.
* Injured myocardium may be — if –
* Percutaneous coronary intervention [PCI] and thrombolysis
2- NON-STEMI:
* Often bad coronary—
* Still a – in coronary artery
* Often good —
* – likely sudden death
* PCI not as urgent
-pathophysiology: non occlusive thrombus
- presentation ; ST depression , enzymes
- goal : prevent total occlusion
muscle / pump
collateral
reversed
re-perfused
atheroma
lumen
collaterals
less
acute cardiac ischemia can have :
1- no ST elevation:
- cardiac markers not elevated —>
- cardiac markers elevated —>
2- ST elevation:
- cardiac marker elevated leading to –>
unstable angina
non st segment elevation mi ( q wave absent )
STEMI , st elevation infract ( q wave usually present )
