Cardiovascular diseases Flashcards
What is ischaemic heart disease?
Inadequate blood supply to the myocardium
What are the main causes of ischaemic heart disease?
- Atherosclerosis and/or thrombus*
- Myocardium hypertrophy due to systemic hypertension
- any imbalance in supply vs demand
At what % occlusion does auto regulation of the coronary arteries breaks down?
75% occlusion
At what % occlusion does auto regulation of coronary arteries break down at rest?
90% occlusion
What happens with acute cardiac ischaemia?
Myocyte dysfunction/death due to blood flow and loss of aerobic metabolism
What is the length of time where damage is reversible with ischaemia?
20-30 mins
At what point in the cardiac cycle doe cardiac perfusion occur?
Diastole
What are the 3 types off angina pectoris?
Stable/typical - fixed dysfunction and predictable symptoms
Variant/prinxmetal - coronary artery spasm - effects less predictable
Crescendo/unstable - red flag - usually due to plaque disruption - worsening symptoms, unpredictable (MI risk = high)
What two syndromes come under acute coronary syndrome?
MI - irreversible damage of myocytes
Crescendo/unstable angina (similar - treated in same way)
There are two types of MI - what are they?
Subendocardial - non full thickness** (most vulnerable region - poorly perfused)
Transmural - regional (kills entire wall)
What is the main characteristic of subendocarial infarction?
Doesn’t need acute coronary occlusion to occur MISMATCH BETWEEN DEMAND AND SUPPLY
- because it is normally poorly perfused, can occur with stable atherosclerotic occlusion of coronary circulation and following a hypotensive episode
What are subendocardial MIs also referred to as?
Non-ST elevation MI
Why are transmural MIs so debilitating?
Death of large region (entire wall) - results in necrosis, fibrosis and formation of fibrous (collagen) scar - cannot pump properly (loss of specialised tissue)
Name the 5 stages of MI morphology (24hrs -6 weeks)
24hrs - normal
1-2 days - pale, oedema with myocyte necrosis and neutrophils
3-4 days - yellow with haemorrhagic edge, myocyte necrosis with macrophage invasion
1-2 weeks - pale, thin (red/grey) - granulation tissue then fibrosis
3-6 weeks - fibrotic scar formation (collagen) (can’t tell how old it is after 4 weeks)
What are the 2 main markers of cardiac damage?
TROPONIN T and I (detectable after 2-3 hrs, peaks at 12, detectable for 1 week)
CREATINE KINASE MB - detectable 2-3h, peaks 10-24 hrs, detectable for 3 days
Also myoglobin (peaks 2hrs) but non-specific - skeletal muscle too
What are the 3 subtypes of creatine kinase
CK MM - skeletal muscle and cardiac
CK BB - brain and lung
CK MB - mainly cardiac but also skeletal
Name some of the complications of MI
- Contractile dysfunction and chronic heart failure
- VF, arrhythmias, sudden cardiac death
- Myocardial rupture
- Ventricular aneurysm
- Mural thrombus - stroke!
- Autoimmune pericarditis (Dressler’s syndrome) (3 day mark - neutrophil inflammatory response)
What is chronic ischaemic heart disease characterised by?
Hypertrophy and dilatation
What can chronic IHD cause?
Sudden death/MI/angina pectoralis on exertion
what is hypercholestroaemia and what are the most common types?
Mutations of genes involved in cholesterol metabolism
LDL receptor (1 in 500) Apolipoprotein B (1 in 1000)
What do individuals with heterozygotic hypercholesterolaemia develop?
- cholesterol deposit (foam cells to endothelium - atherosclerosis)
- tendon, perioccular, corneus arcus, early atherosclerosis
STATINS EFFECTIVE
What are considered abnormal diastolic and systolic BPs?
Diastolic = above 90 mmHg Systemic = above 140 mmHg
What is the effect of hypertension on the heart?
LV hypertrophy without dilatation (initially then subsequent dilatation when it fails to pump blood sufficiently - final stage)
What is the main effect of hypertension on the renal system?
Slow deterioration of renal function - chronic renal failure (damage to vessels - arterial intimal fibroelastosis)
Kidneys have stippled appearance
