Ischaemic Heart Disease

Question 1

What are the areas supplied by the coronary arteries?

Answer 1

• LAD: anterior LV, anteror RV, anterior 2/3 septum
• circumflex: lateral LV
• Posterior descending: posterior and inferior LV, posterior 1/3 septum

Question 2

What factors affect myocardial O2 supply?

Answer 2

• O2 content of blood
• myocardial blood flow
  
  • proportional to perfusion pressure (aortic diastolic pressure)
  • inveresely proportional to vascular resistance
  • subendocardial muscle is most susceptible to ischaemia bc it experiences the greatest pressure
• increased by vasodilation (PGI2, NO)
• influenced by local metabolites (adenosine, lactate, hydrogen ions), vasoconstrictors (endothelin), sympathetic innervation

Question 3

What factors affect myocardial O2 demand?

Answer 3

• ventricular wall stress
  
  • increased myocardial pressure increases stress (hypertension, aortic stenosis)
  • increased radius increases stress (dilation)
  • decreased if wall thickens (LVH)
• heart rate
• contractility

Question 4

What are acute coronary syndromes?

Answer 4

• unstable angina
• sudden cardiac death
• myocardial infarction

Question 5

What are chronic coronary syndromes?

Answer 5

sometimes referred to as ischaemic heart disease

• stable angina
• chronic cardiac failure
• some arrhythmias

Question 6

stable angina

Answer 6

• pain from acute ischaema on exertion
• can be due to chronic vessel narrowing/fixed vessel narrowing, ~70%
• may be accompanied with minor degree of left ventricular failure causing pulmonary congestion and shortness of breath

Question 7

unstable angina

Answer 7

• ischaemic pain at rest, increased frequency and duration
• no infarction
• thrombus formation
  
  • acute narrowing
  • rupture
  • coagulation cascade activation
  • thromboxane A2 secretion by platelets (vasoconstriction)

Question 8

myocardial infarction

Answer 8

• acute plaque event with thrombus formation (99%)
• narrows or occludes the vessel
• acute ischaemia
  
  • ATP depletion
  • ROS generation
  • +Ca2+
  • causes myocyte death after 20-40mins
• full infarct is transmural, 6-8 hours after onset
• usually subendocardial, regional (area supplied by blocked vessel)
• circumferential if triple-vessel coronary narrowing w/severe ischaemia
• can also occur in shock if BP drops following haemorrhage, coronary perfusion drops

Question 9

What are the cardiac markers for MI?

Answer 9

• cardiac troponin (elevated: 3-4 hours, peak: 36 hours, normal: 10-14 days)
• myocardial creatine kinase (elevatied: 3-4 hours, peak: 24 hours, normal: 4 days)

Question 10

sudden cardiac death

Answer 10

• unexpected fatal event
• occurs within 1 hour of symptoms, or with no symptoms
• healthy w/o predictive severe desease
• most sudden deaths
• due usually to coronary disease (atherosclerosis)
• can be caused by large pulmonary embolism
• in 25% first indication of atherosclerosis or IHD
• if resuscitated, usually no infarct

Question 11

What is the pathophysiology of sudden cardiac death?

Answer 11

• automaticity of diseased ventricular myocardium
• wave propogation of ventricular impulses is impeded by diseased muscle
• may initiate intraventricular re-entry
• abnormalities of repolarization

Question 12

What are the possible mechanisms of sudden cardiac death?

Answer 12

• arrhythmic cardiac arrest
  
  • VF due to acute ischaemia in LV myocytes, leading to dysfunction of Na/K pumps causing electrical instability
  • asystole, v-tach
  • myocardial scarring, myocarditis (viral), ischaemia in hypertrophied myocardium
• mechanical
  
  • blood in pericardial sac causing tamponade w/pulseless elctrical activity (ECG shows QRS but there is no CO)

Question 13

What are the morphological changes over time post-MI?

Answer 13

• 12 hours: pale
• 1-2 days: creamy, whitish yellow, may be some haemorrhage and vasodilation from inflammation
• 6-8 weeks: more anr more scar tissue, thinned wall

Question 14

What are the histopathological changes over time post-MI?

Answer 14

• 1 day: dead fibres more eosinophilic, some neutrophils
• 2 days: more neutrophils, nuclei karyolyse/fade
• 1-2 weeks: granulation tissue
• months: fibrous scar w/few capillaries, not many cells, few fibroblasts

Question 15

What are the morphologic complications of MI?

Answer 15

• fatal arrhythmia
  
  • v-fib, f-tach - no blood moving through
  • w or w/o infarct
• cardiac failure within a few hours
  
  • leads to pulmonary congestion and dyspnea
• thrombus formation in LV
  
  • endothelial damage, local changes in flow
  • can embolise, cause cerebral infarct
• pericardial inflammation
  
  • vasodilation and fibrinous exudate (1-2 days)
  • can cause chest pain
• muscle rupture of LV
  
  • tamponade, sudden cardiac death
• papillary rupture, septal rupture
  
  • mitral incompetence
  • failure
  • murmur

**ruptures likely occur at maximal weakeness before collagen is deposited (within 1-10 days)

• aneurysm w/thrombus of LV
  
  • doesn’t rupture, impedes contraction causing failure

Question 16

What are the contributors to IHD?

Answer 16

• atherosclerosis
• myocardial hypertrophy

Question 17

What are the consequences of MI?

Answer 17

• fatal arrhythmia ie v-fib, v-tach, asystole (within an hour or two)
• cardiac failure (within a few hours)
  
  • acute pulmonary oedema, cardiogenic shock
• thrombus in LV over endothelial injury
  
  • embolise to a cerebral infarct
• pericarditis (fibrinous inflammation, ~2 days)
• rupture of LV wall (1-10 days)
  
  • tamponade
• papillary rupture (1-10 days)
  
  • mitral incompetence
• aneurysm with thrombus in LV (weeks to months)
  
  • heart failure (don’t usually rupture)

Question 18

What are the immediate consequences/within a few hours of MI?

Answer 18

• arrhythmias
  
  • v-tach, v-fib, asystole, condiction defects, a-fib
  • acute cardiac failure
    
    • +/- pulmonary oedema, cardiogenic shock

Question 19

What are the consequences of MI within a few days?

Answer 19

• progressive cardiac failure
• rupture (1-10 days) of free wall, IV septum, or papillary muscle
• LV mural thrombus formation over altered endothelium
  
  • potentoal embolic complications
• arrhythmias
• infarct expansion
• fibrinous pericarditis
• papillary muscle dysfunction

Question 20

What consequences of MI develop over months to years?

Answer 20

• ongoing cardiac failure
• arryhthmias
• LV aneurysm
  
  • +/- thrombosis
• papillary muscle dysfunction

Question 21

What determines the size of an infarct?

Answer 21

• which artery (eg LAD supplies most muscle, RCA supplies AV tf can get heart block)
• duration of occlusion
• previous development of collaterals

Question 22

What causes coronary artery occlusion?

Answer 22

• majority of IHD related to atherosclerosis and minor thrombus
• thromboemboli from heart
• vasculitis (immune disorder, causing thrombosis)
• aortic dissection

Question 23

IHD in normal arteries may be related to

Answer 23

• LV hypertrophy
  
  • impairs diastolic perfusion
  • stiffens ventricle
• rapid tachycardias
• hypoxaemia
• shock (low blood volume)

Question 24

What is the management for IHD?

Answer 24

• lifestyle modifications
• nitrites, beta-blockers, Ca2+ channel blockers, ACE inhibitors, anti-platelet agents, fibrinolytics, anticoagulants, lipid-lowering drugs
• stents
• coronary artery bypass