imaging in acute coronary syndromes

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

0 h/1h rule-in & rule-out algorithms

0 h/ 3h rule-out algorithm of

NSTEACS

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

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

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

imaging in acute coronary syndromes

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