Lab investigation of cardiac disease Flashcards
1
Q
What are cardiac markers?
A
- Located in the myocardium
- Released in response to cardiac overload, cardiac injury and cardiac failure
- Can be measured in blood samples
2
Q
What can we use cardiac markers for?
A
- Rule in/out an acute MI
- Confirm an old MI (present to A&E days later)
- Help to define therapy
- Monitor success of therapy
- Diagnosis of heart failure
- Risk stratification of death
3
Q
What makes a good marker?
A
- Analytical - cost-effective, simple to perform, quick, precise and accurate
- Clinical - easy detection of disease, sensitivity vs specificity, prognostic value, ability to improve pt outcome
4
Q
Why is CHD so bad?
A
- 82.5k deaths a year
- 10 deaths an hour!
- Blockage of the coronary arteries through plaque build up - causes occlusion of a vessel
- Not enough oxygen to the heart muscle and tissue = necrosis
5
Q
How do atheromatous plaques develop?
A
- Initial lesions to complicated lesions
- From first decade, you can see beginnings of lipid accumulation
- Macrophages infiltrate and you get development of foam cells
- Ongoing inflammation causes a build up of the lipid core which can become calcified - hardened arteries
- Significant plaque build up will cause complete occlusion and ongoing thrombosis -> cell death and necrosis
6
Q
Chronic vs acute CHD
A
Chronic ischaemic heart disease - stable angina, variant angina, silent myocardial ischaemia
- chest pain but not significant for an MI
Acute coronary symptoms
- unstable angina
- NSTEMI
- STEMI
7
Q
How can angina lead to a heart attack?
A
- Angina from a plaque with fibrous cap in the coronary artery - still sufficient blood flow
- Cap ruptures, blood clot forms around the rupture blocking the artery -> heart attack - significant blockage for necrosis
8
Q
What is important to define the type of CHD?
A
Have very different treatment, prognosis and management
9
Q
Give 7 causes of chest pain
A
- Broken rib
- Collapsed lung
- Nerve infection (shingles)
- Pulled muscle
- Infection
- Heary burn
- Pericarditis
- Pulmonary embolism
- Angina
- MI
10
Q
How do we assess CHD?
A
- medical history
- risk factors
- presenting signs and symptoms
- ECG
- biomarkers
- imaging/scans
11
Q
STEMI VS NSTEMI
A
- An ST elevated MU is caused by complete obstruction of a coronary artery, causing damage that involved the full thickness of the heart muscle
- A non-ST elevation MI is caused by partial obstruction of a coronary artery, and causes damage that doesnt involve the full thickness of the heart wall
12
Q
What is the criteria for acute MI?
A
- Evidence of myocardial necrosis with acute ischaemia
- detection of rise and/or fall of cardiac biomarker values (troponin)
- symptoms of ischaemia
- New or presumed new ST-T changes or new left bundle branch block
- Development of pathological Q waves in ECG
- Imaging of new loss of viable myocardium
- Identification of intraoronary thrombus by angiography or autopsy
13
Q
How long does it take for ischaemic cells to die in myocardial injury?
A
- irreversible injury typially requires 30 mins of ischaemia
- High risk that 80% of cardiac cells within 3 hours, almost 100% by 6 hours
- Cellular contents leak out through membrane, dependent on size and solubility
- Conc gradient from inside to outside is important
14
Q
What cell constituents leak out first in MI?
A
- Ions (e.g. K, P) leak out first, small components can leak out without membrane damage - ATP pump failure
- Metabolites (e.g. lactate or adenosine) are slightly larger, peaks after 1 hr
- Macromolecule start to leak out after 6 hours when the membrane starts to break down - peaks around 2 hours
15
Q
What are the markers of myocardial damage?
A
- Cardiac specific markers troponin-T and troponin=I
- Creatine kinase increased 90% MIs, but less specific as also released from skeletal muscle
- Heart-specific isoforms of creatine phosphokinase (CPK-MB)
- Myoglobin raised early but has short duration - less specific for heart damage
