Flashcards in L48 – Myocardial Ischaemia Deck (49):
Anatomy of the myocardium.
Describe cardiac muscle cells? (B,A,S)
Compare the amount of mitochondria in cardiac muscle cell vs skeletal muscle. Why?
Contain 10x more mitochondria per muscle cell than skeletal muscles
extremely dependent on aerobic metabolism > need
constant supply of a lot of energy
How do coronary arteries penetrate myocardium?
arise from aorta > runs
epicardially > branches penetrate myocardium as
During which phase of the cardiac cycle does blood flow to myocardium?
Blood flow to myocardium occurs only during ventricular diastole:
When microcirculation in myocardium not compressed by cardiac contraction
How does elevated HR protect the heart from overworking?
Faster heart rate > shorter diastolic time (needs more
blood supply for oxygen, energy; but actually getting less) > stops heart from overworking
Which part of endocardium has limited supply?
endocardium in direct contact with oxygenated blood in left ventricle
Branches of Left coronary artery?
Left marginal, Left circumflex, Left anterior descending (LAD)
Branches of Right coronary artery?
Right marginal, Posterior interventricular Artery, Sinoatrial nodal artery
What structures do Left anterior descending artery supply?
Most of heart apex
Anterior wall of left ventricle
Anterior 2/3 of ventricular septum
What structure does Left circumflex supply?
Lateral wall of LV
What structures does right coronary artery (dominant) supply?
Posterior 1/3 of ventricular septum
Posterior-basal wall of left ventricle
What method is used to detect which CA is blocked in heart?
Define Ischaemic heart disease (IHD)?
a group of closely-related syndromes that result from myocardial ischaemia
What is the most likely cause of IHD?
Due to Coronary obstruction > reduction in coronary blood supply
What classifies as coronary obstruction?
One or more leasions that causes at least 75% reduction of cross sectional area of at least one of the major epicardial arteries
What is the effect of ischaemia on myocytes within seconds of MI?
Onset of ATP depletion
What is the effect of ischaemia on myocytes within minutes of MI?
<2 mins = loss of contractility
continuous reduction of ATP
Irreversible damage within 20-40 mins
What is the effect of ischaemia on myocytes after one hour of MI?
Microvascular injury (capillary network in heart is damaged)
How does MI change the rhythm of heart beat within minutes?
1) Cardiac arrhythmias
2) Asystole (heart ceases to beat)/ ventricular fibrillation
How does MI cause contractile dysfunction in heart?
myocytes cannot successfully compensate lack of O2 > dead myocytes cannot conduct electrical impulses / lead to short-circuiting > contractile dysfunction
What is angina pectoris caused by?
symptom complex caused by transient myocardial ischaemia
Does Angina pectoris classify as MI?
Angina pectoris does not induce cellular necrosis > not defined as MI
What is stable angina?
Chronic stenosing coronary atherosclerosis (Fixed coronary obstruction) becoming critical > leave heart vulnerable to increased demand
What is stable angina typically relieved by>?
What is unstable angina?
Pain occurs with progressively
Tends to be more prolonged
What is unstable angina associated with?
Disruption of previously stenosing atherosclerotic plaque
Superimposed thrombosis, Embolism or Spasm
Predictor of MI
What 3 processes can lead to disruption of atherosclerotic plaque?
Hemorrhage into atheroma > expand plaque volume
Rupture / Fissure
Erosion / Ulceration
> Expose thrombogenic plaque constituents
What is the difference in coronary obstruction between stable angina and chronic IHD?
Stable angina = fixed coronary obstruction
Chronic IHD = SEVERE fixed coronary obstruction
What is the difference in coronary obstruction between unstable angina and acute transmural MI?
Unstable angina: Mural thrombus with variable obstruction
Acute transmural MI: Occlusive thrombus
How does vasoconstriction contribute to plaque fracture?
Increase local mechanical forces > contribute to plaque fracture
What is vasoconstriction stimulated by?
1) Circulating adrenal agonist
2) Locally-released platelet contents
3) Impaired secretion of endothelial cells relaxing factors
4) Mediators released from pervascular inflammatory cells
What is the clinical manifestation of angina pectoris progressing to sudden cardiac death?
Angina pectoris (stable or stable > unstable) > MI > either Chronic myocardial ischaemia or sudden death
What are the biomarkers of MI?
Lactate dehydrogenase (LDH)
Creatine kinase + isoenzymes (CK, CK-MB)
Troponin I & T
Aspartate aminotransferase (AST)
What ECG changes can be observed in MI?
ST elevation (in STEMI )
T wave inversion
Enlarged Q wave
Apart from angiogram, ECG, what other diagnostic tools are there for MI?
MRI, Radioistope studies
What does Echocardiogram visualise?
Non-contracting part of ventricular wall + Ejection fraction in ventricle
Which 2 diagnostic tools are not used in acute MI?
What is the extent of ischaemic necrosis in Transmural infarction?
Involves (nearly) full thickness of ventricular wall
What is the extent of ischaemic necrosis in Subendocardial infarction?
Limited to inner 1/3 - 1/2 of ventricular wall
(most distant from blood supply)
Recall: dominant artery gives rise to posterior
descending branch (i.e. supplies the posterior
1/3 of interventricular septum)
Compare the perfusion territory affected by transmural vs subendocardial infarction?
Transmural = perfusion territory in distribution of single coronary artery
Subendocardial = May extend laterally beyond perfusion territory of single coronary artery
What is transmural infarction caused by?
Chronic coronary atherosclerosis
> Acute plaque change
> Superimposed completely obstructive thrombosis
What is subendocardial infarction caused by?
Diffuse stenosing coronary atherosclerosis
How is MI caused in patients with normal coronary arterial supply? (uncommon)
Increased HR or increased heart size
> increased demand of energy from heart
What causes increased HR?
Thyrotoxicosis > increased metabolic state
Stress, anxiety states (shock)
How does chronic hypertension lead to change in heart size?
chronic hypertension (heart needs to work against higher pressure) > cardiomegaly, cardiomyopathies > hypertrophy
How does myocardial rupture arise from MI?
Infarct > zone of necrosis extends > replaced by dense collagenous/ fibrous scar > weakened myocardial wall bulges out > rupture
What are 3 distinctive microscopic changes oberved in MI 4-12 hours after?
Early coagulative necrosis
What are 3 distinctive microscopic changes oberved in MI 12-24 hours after?
Pyknosis of nuclei (dense haematoxylinophilic mass of chromatin)
Hypereosinophilia (different staining property: opaque “tombstone”)
Early neutrophilic infiltrate