L48: Pathogenesis Of Ischaemic Heart Disease Flashcards
Myocardium in contrast to skeletal muscle
Contain much more (10x) mitochondria
—> extremely dependent on aerobic respiration
—> do not need to rest
—> need constant supply of energy
Coronary arterial blood flow
- occurs during Ventricular diastole
- ↑ HR —> ↓ diastolic time —> ↓ Coronary supply —> pain —> prevent overbeating (safety mechanism)
- one way street flows
- limited supply available to endocardium in direct contact with oxygenated blood in left ventricle —> endocardium more vulnerable to ischaemia
Coronary arteries
Left:
- Left Anterior Descending (LAD): Apex, anterior LV, anterior IV septum (2/3)
- Left circumflex: lateral LV
Right:
- Right Coronary Artery (give rise to Posterior Descending): RV, posterior LV, posterior IV septum (1/3)
Ischaemic Heart Disease causes
- Decrease in supply: Reduction in coronary blood flow
—> Coronary obstruction (90%)
—> at least 75% reduction in CSA of one of major epicardial arteries
—> classical symptom: Angina pectoris
—> may lead to sudden death - Increase in demand:
—> increased HR: Thyrotoxicosis, stress, anxiety
—> increased Heart size: Hypertrophy, chronic hypertension, Cardiomegaly
Overall —> myocardial ischaemia
Effect of ischaemia on myocyte
- ATP depletion
- Loss of contractility
- Irreversible injury (Infarction)
- Microvascular injury
Myocyte death:
- cannot conduct electricity —> arrhythmia —> ECG changes
- cannot contract —> decreased ejection fraction + lowered BP
Acute effects of myocardial infarction:
- Leakage of cell contents
- Contractile dysfunction
- Arrhythmia
- Pericarditis (inflammation of pericardium)
- Cardiac rupture
***Clinical manifestation of myocardial ischaemia
- Angina pectoris
- Myocardial infarction (necrosis)
- Chronic ischaemic heart disease (Progressively heart failure secondary to infarction)
- Sudden cardiac death
Angina pectoris (Stable vs Unstable)
- Symptom complex
- caused by TRANSIENT myocardial ischaemia
- not yet necrosis / infarction
- Stable vs Unstable
Stable angina:
- stable chronic stenosing coronary atherosclerosis —> vulnerable to increased demand
- relieved by rest / vasodilator
Unstable angina:
- unstable disrupted atherosclerotic plaque + thrombosis / embolism / spasm
- pain occurs with increasing frequency + more prolonged
- predictor of infarction
Acute plaque changes
Disruption of plaque due to:
- Haemorrhage into atheroma (↑ plaque volume) (未穿)
- Rupture of fibrous cap exposing thrombogenic constituents —> more occlusion
- Erosion of fibrous cap exposing thrombogenic constituents —> more occlusion
—> leading to Acute Coronary Syndrome:
- Unstable angina: Mural thrombus with variable obstruction / Embolism
- Myocardial Infarction: Occlusive thrombus (成個塞左)
- Subendocardial (1/3 - 1/2)
—> may extend laterally beyond perfusion territory of coronary artery
—> DIFFUSE stenosing coronary atherosclerosis - Transmural myocardial infarction (full thickness)
—> within distribution of single coronary artery
—> COPLETELY OBSTRUCTIVE thrombosis / CHRONIC coronary atherosclerosis
Vasoconstriction in ischaemic heart disease
Stimulated by:
- Adrenal agonist
- platelet contents
- impaired secretion of endothelial relaxing factor (Nitric Oxide)
- Mediators from Perivascular inflammatory cell
Result:
- Compromise lumen size
- Shear mechanical force —> Plaque rupture
Diagnosis of myocardial infarction
- Laboratory detection:
1. Potassium
2. Lactate dehydrogenase
3. Creatine kinase MB
4. Troponin I and T - ECG changes:
1. ST elevation
2. Inversion of T waves
3. Increased Q wave amplitude - Echocardiogram: visualise non-contracting part + ejection fraction
- Cardiac catherterisation: allow intervention with plaque as well
- Radioisotope
- Magnetic resonance imaging (MRI)
Consequence of myocardial infarction
- Dead myocyte not replaced
- Re-modelling and re-shape —> Fibrosis
- risk of heart failure + arrhythmia
