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NSTEMI.pptx
1. Management of acute coronary syndromes in patients
presenting without persistent ST-segment elevation
(2020 ESC Guidelines )
Presented by
Dr. Enas Fathy
3. Definition of myocardial infarction
• the detection of an increase and/or decrease of a cardiac biomarker,
preferably (hs-cTn) T or I, with at least one value above the 99th
percentile of the upper reference limit and at least one of the
following:
(1) Symptoms of myocardial ischaemia.
(2) New ischaemic ECG changes.
(3) Development of pathological Q waves on ECG.
(4) Imaging evidence of loss of viable myocardium or new regional wall motion
abnormality in a pattern consistent with an ischaemic aetiology.
(5) Intracoronary thrombus detected on angiography or autopsy.
4. Types of MI
• Type 1 MI:
atherosclerotic plaque rupture, ulceration, fissure, or erosion with
resulting intraluminal thrombus in one or more coronary arteries
leading . to decreased myocardial blood flow
• Type 2 MI: in which a condition other than coronary plaque instability
causes an imbalance between myocardial oxygen supply and demand.
• Types 3 MI: (MI resulting in death when biomarkers are not available)
• Types 4 and 5 MI: related to PCI and coronary artery bypass grafting
(CABG).
5. Epidemiology
• . The proportion of patients with NSTEMI in MI surveys increased
from one third in 1995 to more than half in 2015.
• The use of early angiography ( <_72h from admission increased from
9% in 1995 to 60% in 2015.
• The main consequences of these changes are a reduction in 6-month
mortality.
6. Diagnosis
Clinical presentation
(NSTE-ACS) patients may have the following presentations:
• Prolonged (>20 min) chest discomfort at rest.
• New-onset (de novo) (<3 months) angina (class II or III of the CCSC)
• Recent destabilization of previously stable angina (crescendo angina).
• Post-myocardial infarction (MI) angina.
Typical chest discomfort
Atypical presentations
7. Physical examination
• Usually unremarkable
• Signs of heart failure or haemodynamic or electrical instability
• systolic murmur due to ischaemic mitral regurgitation or aortic stenosis
• signs of non-coronary causes of chest pain
• precipitating conditions such as anaemia and thyrotoxicosis.
EG: -
- Differences in blood pressure between the UL and LL or between the arms
- irregular pulse, jugular vein distension, heart murmurs, friction rub, local
tenderness
- Pallor, sweating, or tremor
8. Diagnostic tools
ECG
Biomarkers:
• high-sensitivity cardiac troponin
• Other biomarkers:
CK-MB, myosin-binding protein C, copeptin, eGFR ،glucose, and (BNP), D-dimer.
Rapid ‘rule-in’ and ‘rule-out’ algorithms
Non-invasive imaging
Differential diagnosis
18. Caveats of using rapid algorithms
• Algorithms should only be used in conjunction with all available
clinical information.
• The ESC 0 h/1h and 0 h/2 h algorithms apply to all patients
irrespective of chest pain onset.
• late increases in cardiac troponin have been described in 1% of
patients, serial cardiac troponin testing.
22. Non-invasive imaging
Functional evaluation
• Transthoracic echocardiography :
- 2D Echo: wall motion abnormalities, EF
- Contrast echocardiography: impaired myocardial perfusion detected
- Strain and strain rate imaging: regional function
Has diagnostic and prognostic value.
detecting alternative pathologies
23. • stress imaging
A- stress echocardiography
B- CMR :
- perfusion and wall motion abnormalities
- detection of scar tissue (using LGE) and can differentiate this from
recent infarction.
- facilitate the differential diagnosis between infarction, myocarditis, or
Takotsubo syndrome, among others.
C- SPECT
24. Anatomical evaluation
CCTA :
- visualization of the coronary arteries
- a normal scan excludes CAD.
- CCTA has a high NPV to exclude ACS
- For PTs with low-to-intermediate pre-test probability for ACS
30. Risk assessment and outcomes
• Electrocardiogram indicators
• Biomarkers
• Clinical scores for risk assessment
• Bleeding risk assessment
31.
32.
33. Biomarkers
• Toponin: The higher the hs-cTn levels, the greater the risk of death.
• Serum creatinine and eGFR.
key elements of (GRACE) risk score
• natriuretic peptides [BNP and N-terminal pro-BNP (NT-proBNP)]
34. Clinical scores for risk assessment
the GRACE risk score:
estimate the risk of in-hospital death.
- Age
- systolic blood pressure
- pulse rate
- serum creatinine
- cardiac arrest at admission
- elevated cardiac biomarkers
- ST-segment deviation
- Killip class at presentation
38. Bleeding risk assessment
• Major bleeding events are associated with increased mortality in NSTE-ACS.
• ARC- HBR
• Integrating ischaemic and bleeding risks.
• tailor antithrombotic duration, intensity.
• to maximize ischaemic protection and minimize bleeding risk in the individual patient.
DAPT duration:
• PRECISE-DAPT score is at patient discharge.
• DAPT score is a bleeding risk estimation to be calculated at 1 year from the index event.
67. Pattern of coronary artery disease in NSTEMI
• 20% of patients presenting with NSTE-ACS have no obstructive lesions of
the epicardial CA.
• 40-80% of patients with obstructive CAD have multivessel CAD.
• 5% - 10% Bypass graft failures and left main CAD, respectively.
• Up to 40% of PT LAD is the most frequent culprit vessel.
• Culprit lesions in NSTE-ACS are more often located within the proximal and
mid segments.
68. How to identify the culprit lesion?
At least two of the following suggestive of acute plaque rupture should be present:
1) Intraluminal filling defects consistent with thrombus.
2) Plaque ulceration (i.e. presence of contrast and hazy contour beyond vessel lumen
3) Plaque irregularity (i.e. irregular margins or overhanging edges), dissection, or impaired
flow.
ECG, Echocardiography, or left ventricular (LV) angiogram may help to identify the
culprit lesion corresponding to a regional wall motion abnormality.
69. Conservative treatment
• Patients who are not candidates for invasive coronary angiography
- advanced age
- chronic kidney disease (CKD)
- prior heart failure/revascularization
- history of cancer
- frailty
• Patients with CAD not amenable To revascularization
- diagnosed with severe CAD who are not amenable to any type of revascularization
- Aggressive 2nd prevention treatment with potent antiplatelet therapy and anti-anginal agents, taking their
comorbidities into account.
70. Pharmacological treatments
A- Antithrombotic treatment
• Antiplatelet drugs and pre-treatment
• Peri-interventional anticoagulant treatment
• Peri-interventional antiplatelet treatment
• Post-interventional and maintenance treatment
B- Treatment of ischaemia
C- Managing oral antiplatelet agents in patients requiring long-term
OAC
D- Management of acute bleeding events
Non cardiac causes e.g. pulmonary embolism, acute aortic syndromes, myopericarditis, aortic stenosis) or extracardiac pathologies (e.g. pneumothorax, pneumonia, or musculoskeletal diseases
troponin rise rapidly (i.e. usually within 1 h from symptom onset if using high-sensitivity assays) after symptom onset and remain elevated for a variable period of time
B-type natriuretic peptide (BNP) provide incremental . prognostic information and may therefore help in risk stratification
This algorism only for heamodynamically stable pt
Cut-offs are assay specific
Alternatives: acute aortic dissection, pericardial effusion, aortic valve stenosis, hyper- trophic cardiomyopathy, mitral valve prolapse, or right ventricular dila- tation suggestive of acute pulmonary embolism.
SPECT: Combined stressrest imaging and/or stress-only imag- ing may further enhance assessment of ischaemia,
fixed perfusion defects suggestive of myocardial necrosis,