Investigation of Cardiac Diseases Flashcards
Acute Coronary Syndrome
Unstable Angina
- minor plaque rupture/ thrombus that doesn’t completely occlude blood flow
- chest pain at rest, no ECG or cTn changes
NSTEMI
- non-full thickness infarction (subendocardial)
- not typical ECG, have cTn changes
STEMI
- transmural infarction
- typical ECG change and cTn change
Classification of MI
Type 1: ischaemic myocardial necrosis secondary to plaque rupture (ACS)
Type 2: ischaemia not due to ACS (supply/demand mismatch)
Type 3: sudden cardiac death
Type 4: procedure related e.g. PCI, stent thrombosis
Type 5: CABG related
Criteria for Type 1 MI
- RISE/FALL of cTn values with at least one value above the 99th percentile URL AND with at least one of the following:
- symptoms of AMI
- new ischaemic ECG changes
- development of pathological Q waves (late event)
- imaging evidence of new loss of viable myocardium or motion abnormality consistent with ischaemia
- coronary thrombus seen on angiography
Criteria for Type 2 MI
Same as type 1 except
- need evidence of oxygen supply and demand imbalance which is unrelated to acute coronary athero-thrombosis
- no coronary thrombus finding
Pathophysiological mechanisms of Type 2 MI
Supply and demand imbalance
Reduced perfusion:
- fixed CAD lesion
- coronary spasm
- embolism
- coronary artery dissection
- severe bradyarrhythmia
- resp failure
- severe anaemia
- hypotension/shock/hypoxia
Increased demand:
- sustained tachyarrhythmia
- severe hypertension +/- LVH
Myocardial injury vs Myocardial infarction
Injury = increased cTn >99th percentile
e.g. heart failure, myocarditis, cardiomyopathy, CKD, PE, stroke
Infarction = clinical evidence of ischaemia and rise/fall of cTn >99th percentile
Approach to elevated cTn values
Stable elevation of cTn
–> chronic myocardial injury e.g. structural heart disease e.g. LVH or dilation, CKD, AF, HF
cTn rise and/or fall
–> with acute ischaemia (symptoms, ECG) = AMI either Type 1 or Type 2
–> without acute ischaemia = acute myocardial injury e.g. acute heart failure, myocarditis
Cardiac Tn: specificity, cutoff value
Sarcomeric protein that regulates muscle contraction
(T-I-C complex bound to myosin)
cTnI and cTnT = cardiac specific isoforms
cTnC non-specific so not used
Cutoff value: 99th percentile used as upper limit of normal (c.f. 97.5 used for most tests e.g. Na, K)
==> high specificity and sensitivity (clear separation of normal and AMI values)
==> exact cutoff is assay specific
Interpretation of cTn, indications for treatment, pitfalls
Serial measurements taken (0,3,6 hrs)
–> additional measurements needed even if initial values are normal!! (possible if present early)
–> most important is CHANGE (50% from baseline)
(in patient with no ECG changes/atypical presentation and no change from baseline after 3 hrs – can exclude ischaemia and NSTEMI; but may still have unstable angina)
–> first measurement >5x 99% => TREAT
–> STEMI on ECG => IMMEDIATE REPERFUSION
Use of high sensitivity cTn is preferred
Peaks within 2 days of AMI, returns to baseline over 5-14 days
Avoiding misinterpretation:
- always in context of clinical setting
- remember rising cTn may not always be AMI – can be PE, myocarditis etc; can be non-cardiac causes
- late presentation of MI –> cTn may not appear to be changing (near peak or gradual downslope)
- elevation of cTn can be chronic e.g. CKD
- analytical interference
(cTn will be very high after PCI due to washout effect of reperfusion)
- cTn is predictor of adverse outcome in chronic HF (higher level = greater risk of MI)
Approach to cardiac marker abnormality
Test validity
Test abnormality
Exclude non-AMI causes e.g. PE, CKD, heart failure, myocarditis
Consider AMI (ECG, symptoms, imaging)
Acute and emergency treatment
Chronic and long term treatment (risk factor modification, anti-platelet, antianginal)
Monitoring
ANP and BNP
ANP
- from atria mainly and ventricles
- response to volume expansion (increase Na and H20 excretion)
BNP (brain/b-type)
- mainly expressed from heart
- increases drastically in ventricular disease
- proBNP cleaved into BNP (active) and NT-proBNP (inactive)
Biological effects of natriuretic peptides and clinical uses
Inhibit RAAS: renal excretion of Na and water
– lower BP
Inhibition of endothelin
– vasodilation
Degree of elevation of BNP correlates with cardiac filling pressures, extent of LV dysfunction, severity of symptoms and worse outcomes in patients with HF
Nesitiride (recombinant BNP) has been marketed for treating acute decompensated HF
Clinical use:
- LV dysfunction
- distinguish HF from other causes of dyspnea
- NOT TO BE USED IN ISOLATION to diagnose HF
- currently not in HA due to cost
Limitations of BNP and NT-proBNP
- more than one cause of dyspnea in a patient – high BNP doesn’t exclude presence of other diseases
- some patients with severe chronic HF may have persistently elevated BNP regardless of treatment
- cor pulmonale due to lung disease a/w increased BNP
- not specific for HF –> LVH, myocarditis, CAD, AF, pul HT, acute or chronic renal failure, ascitic liver cirrhosis, sepsis, endocrine disorders
C-reactive protein
Inflammatory marker – infection or major tissue injury
- acute phase protein synthesised by liver
- also produced by unstable atherosclerotic plaques
Activates complement system, enhance macrophage phagocytosis
==> extremely sensitive but non-specific for inflammation
- up to 10,000 fold increase within 6 hrs and peaks at 48 hrs
- declines with t1/2 of 18 hrs after resolution
- have high sensitivity assays
Clinical use of CRP
Concentrations below those seen in infection are a marker of atherosclerotic process
- a/w risk of CAD, ischaemic stroke, vascular mortality and several other diseases
- may be part of CV risk stratification in primary prevention (>10 mg/L = very high risk; 3-10 = high risk; <1 = low risk)
Limitations:
- no routinely used in HA for CVS risk
CVS risk
- for intermediate risk patients with 10-20% risk from framingham score –> hsCRP > 2-3 may suggest indication for statins
