IMAGING IN ACUTE
CARDIOLOGYPROFESSOR MICHAEL REES
PROFESSOR OF CARDIOVASCULAR STUDIES BANGOR UNIVERSITY
VISITING PROFESSOR CHESTER UNIVERSITY
Acute Coronary Syndromes
Pathophysiology
▪Plaque Disruption
▪ Intravascular Thrombosis
▪ Impaired myocardial blood
supply
Acute Coronary Syndromes
Definitions
▪ MI: Cardiomyocyte necrosis in a clinical setting consistent with
acute myocardial ischaemic.
▪ Criteria for Diagnosis of MI:
▪ Raised cardiac Biomarker + one of the following:
▪ Symptoms of ischaemic
▪ New ischaemic changes on ECG.
▪ Imaging evidence of RWMA or loss of viable myocardium.
▪ Intra coronary thrombus on Angio.
Type 1 MI
• Caused by plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus leading to decreased blood flow and/or distal embolization. Usuallythere is severe underlying CAD.
• In 5-20%, non-obstructive CAD or no angiographic evidence of CAD, particularly in women.
Primary PCI in STEMI
• In our last 95 activations for our primary PCI pathway only 32
proceeded to primary PCI
• ECG changes often non specific
Non Imaging Technique
Flow/Pressure Wire and FFR
▪ FFR technique is a method to determine if an individual lesion or section of vessel is flow limiting
▪ Calculation of FFR any result below 0.75 indicates a significant lesion
▪ Now a ‘grey area’ of results below 0.80 has been introduced
▪ FFR ‘significance’ has been drawn from comparison to imaging and non imaging tests for ischaemia
IFR▪ Instant wave free ratio
▪ Measures ratio of distal
coronary pressure to aortic
pressure
▪ A method of determining
the degree of stenosis of a
lesion without using
adenosine.
▪ Can be used real time
Imaging Technique-Optical
Coherence Tomography
▪ Uses infra-red light to
visualise interior of vessel
▪ Gives detailed architecture
to interior of vessel
▪ Needs contrast to clear
blood from vessel
▪ Useful for measurement of
diameter
▪ Looking at stent apposition
Imaging Technique-Intravascular
Ultrasound▪ Longstanding technique
▪ Images whole of arterial
wall
▪ Does not require
displacement of blood
Type 2 MI
▪ Myocardial necrosis caused by a condition other than coronary plaque
instability: e.g.
▪Spasm, tachyarrhythmias, bradyarrhythmias, anaemia,
respiratory failure, hypotension and severe hypertension.
▪Myocardial necrosis secondary to chemicals and toxins
e.g. septicaemia & major trauma.
Other types of Myocardial
Infarction
▪Type 3 sudden death no Troponin measured
▪Type 4 during PCI: definition is 5x reference level for MI
▪Type 5 during CABG : definition is 10x reference level
for MI
Acute coronary syndromes
Unstable Angina (UA)
▪ Myocardial ischaemia at rest or minimal exertion in the absence of
cardiomyocyte necrosis i.e. No rise in cardiac markers.
▪ Use of Hs Tn has lead to increase in diagnosis of MI and decrease in
UA.
• Lower risk of death, derives less benefit from intensified antiplatelet
therapy & early invasive strategy.
Non ST Elevation Acute Coronary
Syndromes▪ Initial Assessment of the patient
▪ Troponin T and rule in Rule out algorithms
▪ Risk Stratification
▪ Investigation and Treatment Strategies
▪ Decisions on future therapy
New guidelines for NSTEMI July 2015 European
Society of Cardiology
ACUTE CHEST PAIN
NSTEACS▪ Initial assessment of the patient
▪ Troponin T and the rule in/ rule out algorithms
▪ Risk stratification
▪ Treatment and Investigation Strategies
▪ Future therapy strategies
Initial assessment of the patient
NSTEACS▪ Initial assessment of the patient
▪ Troponin T and the rule in/ rule out algorithms
▪ Risk stratification
▪ Treatment and Investigation Strategies
▪ Future therapy strategies
0 h/1h rule-in & rule-out algorithms
0 h/ 3h rule-out algorithm of
NSTEACS
NSTEACS▪ Initial assessment of the patient
▪ Troponin T and the rule in/ rule out algorithms
▪ Risk stratification
▪ Treatment and Investigation Strategies
▪ Future therapy strategies
Possible non-acute coronary
syndrome causes of Troponin rise▪ Chronic or acute renal dysfunction
▪ Hypertensive crisis
▪ Tachy-or- bradyarrhythmias
▪ Pulmonary Embolism
▪ Inflammatory diseases e.g.. Myocarditis
▪ Acute neurological disease including stroke or subarachnoid haemorrhage
▪ Aortic dissection, aortic valve disease or hypertrophic cardiomyopathy
▪ Cardiac contusion, ablation, pacing, cardioversion or endomyocardial biopsy
▪ Hypothyroidism
▪ Apical ballooning syndrome Tako Tsubo cardiomyopathy
▪ Infiltrative diseases e.g. amyloidosis, haemachromatosis,sarcoidosis, scleroderma
▪ Drug toxicity e.g. Adriamycin, 5-fluorouracil,herceptin, snake venoms
▪ Burns affecting >30% of body surface area
▪ Rhabdomyolysis
▪ Critically ill patients especially with respiratory distress or sepsis
Very High Risk Patients
Very High Risk Patients
▪ High risk patients should be taken to the catheter laboratory within 2 hours of onset of symptoms.
▪ This leaves very little time for non invasive investigations.
▪ Most investigations will be invasive in the lab, angiography, intravascular imaging, FFR and IFR.
▪ Perhaps time for a chest x-ray or echo
▪ Recurrent or ongoing chest
pain refractory to medical
treatment
▪ Life threatening arrhythmias
or cardiac arrest
▪ Mechanical complications of
MI
▪ Acute Heart failure
▪ Recurrent dynamic ST-T
wave changes, particularly
with intermittent ST elevation
Angiographic Diagnosis in
NSTEMI
NSTEMI RCA Rx PCI
Diagnosis with Echo within 2
Hour Window
High Risk
Patients
▪ High risk patients should be
taken to the cardiac catheter
laboratory within 24 hours.
▪ This gives a window of
opportunity for other non invasive
tests
▪ CXR, echo, MRI, Cardiac CT.
▪ Careful use of contrast.
Rise or fall in cardiac Troponin
compatible with myocardial
infarction
Dynamic ST or T wave changes
(symptomatic or silent)
GRACE score >140
HIGH risk
Patients Opportunity to carry out MRI
before transfer to cardiac catheter
laboratory
Diagnosis of Myocardial Infarction
causing Death
Patients with diagnosis of
Myocardial Infarction at Death
NSTEACS▪ Initial assessment of the patient
▪ Troponin T and the rule in/ rule out algorithms
▪ Risk stratification
▪ Treatment and Investigation Strategies
▪ Future therapy strategies
Intermediate Risk Patients
Intermediate
Risk
▪ Diabetes Mellitus
▪ Renal Insufficiency
(eGFR<60mL/min/1.73 mm2
▪ LVEF <49% or congestive heart
failure
▪ Early post infarction angina
▪ Prior PCI
▪ Prior CABG
These patients should undergo
angiography within 72 hours
however for many patients non-
invasive testing would be
preferable or safer.
Intermediate
RiskPatients with grafts may be best
investigated by CT
In some cases patients with
previous PCI may be best
investigated by CT
Contrast usage must be carefully
monitored
Case StudyYoung man with general malaise,
diarrhoea, some chest pain.
Generalised ST changes on ECG
Working diagnosis myo-pericarditis
NSTEACS▪ Initial assessment of the patient
▪ Troponin T and the rule in/ rule out algorithms
▪ Risk stratification
▪ Treatment and Investigation Strategies
▪ Future therapy strategies
Possible non-acute coronary
syndrome causes of Troponin rise▪ Chronic or acute renal dysfunction
▪ Hypertensive crisis
▪ Tachy-or- bradyarrhythmias
▪ Pulmonary Embolism
▪ Inflammatory diseases e.g.. Myocarditis
▪ Acute neurological disease including stroke or subarachnoid haemorrhage
▪ Aortic dissection, aortic valve disease or hypertrophic cardiomyopathy
▪ Cardiac contusion, ablation, pacing, cardioversion or endomyocardial biopsy
▪ Hypothyroidism
▪ Apical ballooning syndrome Tako Tsubo cardiomyopathy
▪ Infiltrative diseases e.g. amyloidosis, haemachromatosis,sarcoidosis, scleroderma
▪ Drug toxicity e.g. Adriamycin, 5-fluorouracil,herceptin, snake venoms
▪ Burns affecting >30% of body surface area
▪ Rhabdomyolysis
▪ Critically ill patients especially with respiratory distress or sepsis
Risk stratification▪ GRACE risk score
▪ Most accurate risk stratification both on admission and at
discharge
▪ http:// www.gracescore.org/WebSite/default.aspx?ReturnUrl=%2f
▪ TIMI risk score
▪ Simple to use, but poor discriminative accuracy than GRACE
▪ http://www.timi.org/index.php?page= calculators
Low Risk Patients▪ Any characteristic not mentioned in any of the higher risk
categories.
▪ This category should be investigated by non invasive imaging
once risk score has been assessed.
Low Risk Patients
Cardiac CTRoutine use in low risk patients
Increasing use in medium and high
risk patients
Imaging technique-Nuclear SPECT
▪ Post intervention chest pain
▪ Multi-vessel disease
assessment of lesion
significance.
▪ Primary diagnosis of
ischaemia
Cardiac Echo
and Stress echoUsed to determine viability in low
dose studies to diagnose
hibernating myocardium
Used to detect ischamia in
ascending dose of dobutamine
Cardiac MRIUsed increasingly in acute cardiac
syndromes
Stress MRI to diagnose ischamia
or hibernating myocardium
Quantification of myocardial
damage
Planning for intervention
Differential diagnosis of chest pain
Conclusions
▪ Evidence from mortality studies indicate diagnosis not always
correct
▪ In acute coronary syndrome ECG changes may be non
specific
▪ Symptoms can vary significantly
▪ Non invasive imaging is therefore of vital importance in
establishing the correct diagnosis in suspected myocardial
infarction
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